Encodes a carboxy-terminal truncated or internally deleted protein.
egg chamber (with aspDD4)
larval brain & neuroblast & aster
larval brain & neuroblast & centrosome
larval brain & neuroblast & mitotic cell cycle
larval brain & neuroblast & spindle
meiotic telophase II & contractile ring
meiotic telophase II & spindle
onion stage spermatid & nucleus
spermatocyte & aster (with aspDD4)
spermatocyte & centrosome
spermatocyte & spindle
spermatocyte & spindle (with aspDD4)
spermatocyte & spindle (with Df(3R)Hdγ1)
Despite exhibiting increased metaphase figures, asp1 mutant brains do not display neuroblast loss.
87.8% of mitotic cells in Spc25mitch-1/Df(3R)ry75 larval brains have overcondensed chromosomes, and the mitotic index is increased compared to wild type. The ratio of mitotic cells in prometaphase/metaphase to those in anaphase/telophase is greatly increased compared to wild type.
98.2% of the ovarioles of homozygous females do not produce eggs. 52.4% of egg chambers have the normal complement of germ cells and 47.5% of egg chambers contain fewer than 16 germ cells. The oocyte nucleus is sometimes missing and is occasionally mispositioned. 97.7% of the ovarioles of asp1/aspDD4 females do not produce eggs. 44.1% of egg chambers have the normal complement of germ cells and 55.9% of egg chambers contain fewer than 16 germ cells. The oocyte nucleus is sometimes missing and is occasionally mispositioned.
Spermatocytes in asp1 homozygotes, asp1/aspDD4 trans-heterozygotes and asp1/Df(3R)Hdγ1 trans-heterozygotes display spindle abnormalities during meiosis I. In late prophase, the majority of spindles are irregular. In metaphase, approximately half of the spindles are irregular. These are defined as spindles exhibiting long and wavy microtubules and/or the absence of distinct bundles of kinetochore microtubules. In late anaphase and late telophase, approximately a third of spindles are irregular, with a proportion of spindles absent. In oocytes of asp1/aspDD4 trans-heterozygotes, meiosis I and II progress normally, however the sperm aster does not increase in dimension as in wild-type. In the asp mutant cytoplasm, the microtubules of the sperm aster never extend to the egg cortex. The sperm aster duplicates as in wild-type but is frequently found to detach from the spindle forming around the haploid male pronucleus.
Most dividing neuroblasts arrest in metaphase in homozygous larval brains. A substantial fraction of the metaphases show precocious centrosome splitting. The astral microtubules are generally shorter and fewer than in wild-type metaphases. Many spindle microtubules are poorly focused and do not appear to terminate at the centrosome. 41% of homozygous spermatids consist of a normal-sized nucleus associated with a normal Nebenkern. 15% contain a normal Nebenkern associated with an abnormally sized nucleus (probably the consequence of a failure in chromosome segregation but not in cytokinesis). 23% have 2 or 4 normal-sized nuclei associated with a single Nebenkern of 2 or 4 times the normal size (the consequence of a failure in cytokinesis but not in chromosome segregation). In addition, spermatids consisting of a single large Nebenkern associated with 2 (12%), 4 (3%) or more than 4 (6%) nuclei of different sizes are seen (probably a consequence of failures in both cytokinesis and chromosome segregation). Asters are smaller than normal during meiotic prometaphase in mutant males and are often not attached to the nuclear envelope (in contrast to wild type). The two asters are usually close to each other, suggesting a delayed migration to the opposite sides of the nucleus. Spermatocytes form abnormally shaped and poorly focused bipolar spindles. The centrosomes do not appear to be attached the ends of these spindles in many cells, but instead float free in the cytosol. Central spindle morphology looks normal in about half of the meiotic telophases in mutant males, but is severely affected in the other half of telophases. The central spindle fails to form completely in a fraction of the abnormal telophases, while in the remaining cells some interzonal microtubules can be discerned that are organised in small and irregular bundles that do not completely traverse the cell. Telophases with abnormal central spindles have a disrupted actin contractile ring.
Postmeiotic spermatogenic stages of asp1 males show a series of alterations due to the abnormal meiotic spindles. The most conspicuous alterations include variable size nuclei and nebenkern of early spermatids. The spermatids are also multinucleate instead of having a single uniform size nucleus. The spermatids are elongated: abnormal size mitochondrial derivatives elongate alongside more than one axoneme. Some spermatids remain syncytial due to failure of the individualization process and are eliminated during the coiling stage.
asp1 homozygous larval brains have a high mitotic index, extremely condensed X-shaped chromosomes and numerous aneuploid and polyploid cells: a fraction of the cells may continue to divide when the maternal gene product for spindle production is exhausted, and mistakes are made in chromosome segregation resulting in high frequencies of aneuploid and polyploid cells. In larvae carrying Df(3R)Su9 and Df(3R)L16 the brain phenotype is similar to asp1 homozygous larvae except aneuploid and polyploid cells are rare and no anaphases are found. Adult escapers have an increase in cuticular defects similar to asp homozygote and male and female sterility. Does not interact with βTub85D.
In asp1 homozygotes the mitotic cycle is arrested in metaphase resulting in a high frequency of polyploid cells. Sex chromosome disjunction during male meiosis is severely affected resulting in diplo and nullo gametes. The meiotic spindles of living cells are morphologically abnormal due to an altered structural component of the spindle other than the tubulins.
Most larvae with small or absent imaginal discs; delayed development; survivors with nicked wings and rough eyes. Males sterile at 18oC and fertile at 25oC; produce abundant MI nondisjunction. Larval neuroblasts frequently polyploid, especially when held at 18oC. Phenotype enhanced by duplications for 97B. Enhanced by: Ts(Y;3Rt)B158 Not enhanced by: Ts(Y;3Rt)R71
asp1 has increased occurrence of cell division | larval stage phenotype, non-enhanceable by rl1
asp1/asp[+] is an enhancer of embryonic/larval cuticle phenotype of baz4
asp1/asp[+] is an enhancer of embryonic/larval cuticle phenotype of bazG0484
The cuticle phenotype of dead embryos derived from baz4/+ embryos derived from a cross of baz4/+ females to wild-type males is enhanced if the females also carry one copy of asp1.
The cuticle phenotype of dead embryos derived from bazG0484/+ embryos derived from a cross of bazG0484/+ females to wild-type males is enhanced if the females also carry one copy of asp1.
rl1 recessively enhances the eye and wing defects associated with the asp1/aspDD3 mutant. rlSu14 and Dsor1Su1 dominantly suppress the morphological defects and sterility of asp1/aspDD3 mutants. The brain neuroblast mitotic index of double mutants with rl1 or Dsor1Su1 is generally as for asp1 mutants alone. The rl1; asp1 double mutant also displays an increase in the number of mitotic figures that show lagging chromatids at anaphase, and a low frequency of abnormal mitotic figures where the telomeric ends of chromosomes appear to remain in contact, forming daisy chains. The frequency of aneuploid and polyploid figures is significantly increased. The asp1; Dsor1Su1 double mutant shows reduction in the frequency of aneuploid and polyploid figures. Survival of embryos from asp1/aspDD3 females is increased in double mutants with Dsor1Su1, fewer have no nuclei.
12% survive to adulthood at 25oC.